Microinjection of ras specific monoclonal antibody has been shown to block cellular DNA synthesis in normal and some transformed cell lines. This antibody also, reverts the transformed morphology of ras NIH 3T3 cells and induces these cells to flatten out taking on the appearance of normal NIH 3T3 fibroblasts. Fibroblast cells have been shown to be dependent upon a ras driven proliferation system. Lymphoid cell lines, macrophages and T cells, were serum starved and induced to proliferate by treatment with either IL-1, IL-2, or CSF. Microinjection of ras specific antibody had no effect upon factor induced cellular proliferation of these lymphoid lines, suggesting that IL-1, IL-2, or CSF induction of cellular growth does not depend upon a ras function. A monoclonal antibody raised against the raf protein has recently been prepared that immunoprecipitates raf specific proteins at 74 and 44 Kd. When micro-injected into NIH 3T3 cells, raf transformed NIH 3T3 cells or ras transformed NIH 3T3 cells the cells are blocked from entering the DNA synthesis phase of the cell cycle. This result suggests that ras and raf proteins are in the same membrane signal transduction pathway and that ras is upstream of the raf serine kinase in the proliferative pathway. The raf and ras antibodies are tools which we can utilize to study the biochemical interrelationships of the ras and raf proteins in cellular hormone induced membrane signal transduction. Bacterial synthesized raf protein was partially purified and microinjected into serum depleted NIH 3T3 cells. Cells in the injected area of the cover slip were found to have entered the DNA synthesis phase of the cell cycle following raf injection, indicating that raf gene product is directly responsible for its transformation.